In the wake of the 9/11 attacks on the World Trade Center (WTC), over 60,000 individuals took part in the rescue, recovery and clean-up efforts. Many of these individuals now face physical and mental health problems, with up to 60% reporting symptoms of post-traumatic stress disorder (PTSD) or lower respiratory symptoms (LRS). Moreover, the rate of co-occurrence between PTSD and LRS is higher than what can be explained by shared risk factors, such as WTC-related exposure. Across 2.5 years, PTSD was shown to increase new onsets of LRS. Despite this evidence, significant gaps in our understanding of the comorbidity remain. In particular, all existing data about PTSD/LRS in WTC responders comes from traditional, clinic-based assessments. These require patients to recall symptoms weeks or months after they occurred, which introduces possible recall biases and conceals the daily prevalence and burden of the symptoms. Moreover, traditional assessments consider only average symptom levels, making it difficult to examine the real time dynamic between PTSD and LRS or to test possible biological pathways between them. PTSD has been linked with exaggerated response to stress and dysregulation of immune system, which may increase vulnerability to medical comorbidities, including pulmonary inflammation and respiratory problems. However, these hypothesized pathways have not been tested. The proposed study will address these gaps in our understanding of PTSD/LRS via ecological momentary assessments (EMA). Unlike traditional measures, EMA was designed specifically to provide data on daily fluctuations of symptoms and biomarkers in medical patients by sampling health status outside the clinic multiple times per day. We will use EMA with WTC responders to 1) establish the daily prevalence and burden of PTSD/LRS in an ecologically valid manner, 2) evaluate the temporal dynamics between PTSD and LRS in real time, testing whether occurrences of PTSD symptoms increase the probability of future LRS, 3) repeatedly sample biomarkers to test pathways linking physiologic stress response, immune dysregulation, and pulmonary inflammation to PTSD and LRS, and 4) evaluate the congruence of retrospective measures of PTSD and LRS with EMA-based estimates and recalibrate traditional clinical measures as needed. Results from the study will provide the first ecologically valid estimates of daily PTSD symptom and LRS prevalence in WTC responders, along with estimates of their burden in daily life. The study also will investigate the direction of PTSD-LRS link in real time and test biological mechanisms that may explain this relationship, which has not been attempted previously. Moreover, daily ambulatory sampling of pulmonary biomarkers will provide a novel perspective on respiratory health of responders. More valid estimates of symptom burden obtained in this study will inform both the policy for managing WTC-related conditions and provision of services to responders. The information on the temporal sequence and biological mediators will help to guide development of interventions to reduce PTSD and LRS burden in WTC-exposed and other traumatized populations.